Our objective is to determine the biochemical basis for the increased responsiveness to glucocorticoids which corticosteroid glaucoma and primary open-angle glaucoma (POAG) patients manifest in their eye and other tissues. Definition of a specific biochemical defect could lead to an understanding of the pathogenesis of these apparently related diseases, to earlier detection of those at risk, and to more rational therapy. We will study in tissue culture trabecular meshwork endothelial cells, peripheral blood lymphocytes, and skin fibroblast from POAG patients, matched controls, and, as available, from persons classified as to ocular corticosteroid responsiveness. In trabecular endothelial cells, we will determine the number of specific glucocorticoid receptors per cell, and the affinity constants, and compare biological responses to glucocorticoids, of POAG patients and controls. Particular attention will be paid to glucocorticoid senstivity of cell growth, and synthesis of glycosaminoglycans and collagen. In peripheral lymphocytes, in which we have demonstrated greater cellular sensitivity to glucocorticoids in POAG patients, but found no abnormality of cytosol glucocorticoid receptors, we will look for possible glucocorticoid effects on cyclic-adenosine mono-phosphate (c-AMP)-dependent protein kinases (enzymes thought to play a role in control of lymphocyte transformation). Fibroblast studied will parallel those in lymphocytes.